Treatment patterns of non-ST-elevation acute coronary syndrome patients presenting at non-PCI centres in the Netherlands and possible logistical consequences of adopting same-day transfer to PCI centres: a registry-based evaluation.

BACKGROUND: European Society of Cardiology (ESC) guidelines recommend same-day transfer to a percutaneous coronary intervention (PCI) centre for angiography in high-risk (ESC-HR) patients with non-ST-elevation acute coronary syndrome (NSTE-ACS). We describe the treatment patterns of NSTE-ACS patients presenting at non-PCI centres and evaluate the logistical consequences of adopting same-day transfer. METHODS: From August 2016 until January 2017, all consecutive NSTE-ACS patients presenting at 23 non-PCI centres in the Netherlands were recorded. We built an online case report form in collaboration with the National Cardiovascular Database Registry to collect information on risk stratification by the attending physician, timing and location of angiography, and treatment. RESULTS: We included 871 patients (mean age 69.1 ± 12.8). 55.8% were considered ESC-HR. Overall, angiography at non-PCI centres was 55.1% and revascularisation was 54.1%. Among ESC-HR patients, angiography at non-PCI centres was 51.4% and revascularisation was 54.9%. Angiography <24 h was 55.6% in patients with angiography at a non-PCI centre and 74.3% in patients with angiography at a PCI-centre. Assuming patients would receive similar treatment, adoption of same-day transfer would increase transfers of ESC-HR patients who undergo PCI (44.3%), but also increases transfers of medically treated patients (36.2%) and patients awaiting coronary bypass artery grafting (9.1%). CONCLUSIONS: In this registry of NSTE-ACS patients at non-PCI centres, the majority of ESC-HR patients underwent angiography at a non-PCI centre. Same-day transfer occurred in one-quarter of the ESC-HR patients, despite guideline recommendation. Nonselective adoption of same-day transfer to a PCI centre would increase transfers of ESC-HR patients who undergo PCI, however, equally increases transfers of patients who are medically treated.

Acute chest pain in a patient treated with capecitabine.

A 61-year-old male with a history of metastatic colorectal cancer was referred to our hospital for primary coronary intervention because of acute ST-elevation myocardial infarction. Coronary angiography, however, revealed no significant stenoses. When asked, the patient revealed that capecitabine (Xeloda(R)) was started by his oncologist one day before admission. It is known that this oral 5-FU analogue drug, used in metastatic colorectal cancer, can cause coronary artery spasms. The main treatment of capecitabine-induced vasospasm is discontinuation of the drug. Indeed, after cessation of the drug the patient remained free of symptoms and the ECG abnormalities normalised. (Neth Heart J 2009;17:288-91.).

[Pearson's syndrome: a multi-system disorder based on a mt-DNA deletion]. / Het syndroom van Pearson: een multisystem disorder gebaseerd op een mt-DNA-deletie.

In 1979 Pearson described a syndrome, in which the main symptoms were severe sideroblastic anemia and exocrine pancreas dysfunction. The aetiology was still unknown. A decade later, the Pearson syndrome can be described as a lethal multisystem disorder, in which the bone marrow and exocrine pancreas show major dysfunction, but also other organs (like kidneys, liver, gut and skin) can be affected. These patients also show growth retardation. The study of the mitochondrial DNA allowed identification of a deletion in the mitochondrial DNA. The case of a patient suffering from Pearson's syndrome is reported.

Flecainide widens the excitable gap at pivot points of premature turning wavefronts in rabbit ventricular myocardium.

INTRODUCTION: The mechanisms by which Class IC drugs slow the rate of functional reentrant arrhythmias are not completely understood. We hypothesized that flecainide widens the excitable gap beyond the pivot point of premature turning wavefronts. METHODS AND RESULTS: In eight perfused subepicardial layers of rabbit left ventricle, a linear lesion was made by radiofrequency (RF) ablation parallel to the fiber orientation. One end of the RF lesion was extended by a short incision. Pacing next to the lesion induced a wavefront propagating with a sharp U-turn around the end of the lesion in either the clockwise or counterclockwise direction. A high-density mapping electrode (240 electrodes, 350-microm resolution) was used to record unipolar electrograms at the pivot point. During control, the shortest V1-V2 interval proximal to the pivot point was 162 +/- 12 msec compared with 173 +/- 13 msec distal to the pivot point (difference 11 +/- 8 msec; P < 0.01). After infusion of flecainide 2 mg/L, the shortest V1-V2 interval proximal and distal to the pivot point were 217 +/- 29 msec and 244 +/- 36 msec (difference 27 +/- 16 msec; P < 0.01). Due to the increase in V1-V2 interval at the pivot point, flecainide widened the temporal excitable gap in the returning limb of the turning wavefront from 30 +/- 11 msec to 55 +/- 22 msec (P < 0.01). High-density mapping at the pivot point revealed that this widening of the excitable gap was due to both macroscopic discontinuous conduction and functional conduction block at the pivot point. CONCLUSION: Flecainide widens the excitable gap in the returning limb of premature U-turning wavefronts by causing macroscopic discontinuous conduction and functional conduction block at the pivot point.

Preferential depression of conduction around a pivot point in rabbit ventricular myocardium by potassium and flecainide.

INTRODUCTION: During reentrant arrhythmias, the circulating wavefront often makes a sharp turn around a functional or anatomic barrier. We tested the hypothesis that lowering the safety factor for conduction by high K+ or flecainide preferentially depresses conduction of sharply turning wavefronts. METHODS AND RESULTS: In 16 Langendorff-perfused rabbit hearts, a thin layer of anisotropic ventricular myocardium was made using a cryoprocedure. In this layer, a linear radiofrequency lesion was made parallel to the fiber orientation. The tip of the lesion was extended by a short incision. U-turning wavefronts were initiated by pacing at one side of the lesion. A mapping electrode (240 electrodes, resolution 350 to 700 microm) was used to measure conduction times and velocity of planar waves (longitudinal and transverse) and U-turning wavefronts. The safety factor for conduction was lowered by high potassium (8, 10, and 12 mmol/L) and flecainide (1 and 2 mg/L). On average, high potassium and flecainide increased the conduction times of U-turning wavefronts 1.6 times more than longitudinal or transverse planar wavefronts (P < 0.01). At a critical lowering of the excitatory current, functional conduction block occurred at the pivot point, which forced the wavefront to make a longer U-turn. In these cases, the total U-turn conduction time increased from 27+/-9 msec to 75+/-37 msec. About 40% of this delay was caused by a shift of the pivot point and consequent lengthening of the returning pathway. CONCLUSION: Lowering the amount of excitatory current by potassium or flecainide preferentially impairs U-turn conduction. The occurrence of long delays and conduction block at pivot points may explain the mode of action of Class I drugs.